Persistence of improvement in insulin sensitivity following a dietary weight loss programme

McLaughlin, Tracey; Schweitzer, Paula K.; Carter, S.; Yen, Chih‐Hsuan; Lamendola, Cindy; Reaven, Gerald M.

doi:10.1111/j.1463-1326.2008.00877.x

Cited by 27 publications

(33 citation statements)

References 33 publications

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“…Interventional effects on insulin resistance are important in obesity: insulin sensitivity improvement is maintained in obese patients for 2-3 years following dietary weight loss if weight is not regained [40]. The observation of a paradoxical increase of insulin sensitivity in animals infected by Ad36 is intriguing and envisages the possibility that a better glycemic control could be achieved in Ad36-infected subjects: expansion of adipose tissue and increase of glucose uptake in skeletal muscle and adipose tissue might lead to better glycemic control in vivo [41,42].…”

Section: Introductionmentioning

confidence: 99%

Adenovirus-36 Seropositivity Enhances Effects of Nutritional Intervention on Obesity, Bright Liver, and Insulin Resistance

et al. 2011

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Ad36 previous infection is significantly associated with enhanced weight loss, bright liver disappearance, and recovery of insulin sensitivity through the chosen tailored nutritional interventional treatment. Nonetheless, Ad36 seronegative NAFLD patients' fatty liver pattern improves, at a lower extent, also without significant weight loss: an effect of dietary changes profile, Mediterranean diet, not only of lowered food caloric intake, is conceivably operating.

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Section: Introductionmentioning

confidence: 99%

Adenovirus-36 Seropositivity Enhances Effects of Nutritional Intervention on Obesity, Bright Liver, and Insulin Resistance

et al. 2011

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“…Dietary fat is preferentially trafficked to adipose and hepatic triglyceride stores rather than being used for energy needs. This enhanced metabolic response to ingested nutrients occurs, in part, from an increase in whole body insulin sensitivity (109,124,142,148,158). While beneficial for metabolic health, the enhanced insulin sensitivity primes the body for rapid, energetically efficient weight gain during chronic overfeeding (148,230).…”

Section: Enhanced Metabolic Flexibility: Improved Nutrient Clearancementioning

confidence: 99%

“…The inflexible state of metabolism results from a discordant attempt of numerous peripheral tissues to respond to changing fuel needs and nutrient availability, yielding little or no discernable response. Metabolic inflexibility is a common characteristic of obesity (119,220), and energy-restricted weight loss reverses many of its associated impairments in metabolic regulation (48,81,158,188,219). Because enhanced metabolic flexibility improves the metabolic response to ingested energy, it alters the peripheral signals of nutrient status that are sent to the brain during weight maintenance and during weight regain (Fig.…”

Section: Enhanced Metabolic Flexibility: Improved Nutrient Clearancementioning

confidence: 99%

“…Reduced leptin levels are more intuitive, as leptin is secreted from adipose tissue. Lower insulin levels can be explained by improved insulin sensitivity (109,124,142,158) and a reduced fasting and postprandial response in glucosedependent insulinotropic polypeptide (121, 238). The low levels of leptin and insulin levels have been traditionally thought to convey a message of "depleted energy" stores to key regulatory areas in the brain (Fig.…”

Section: Adipose Signals: Low Reserves and An Empty Fuel Tankmentioning

confidence: 99%

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Biology's response to dieting: the impetus for weight regain

MacLean

Bergouignan

Cornier

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

374

326

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Dieting is the most common approach to losing weight for the majority of obese and overweight individuals. Restricting intake leads to weight loss in the short term, but, by itself, dieting has a relatively poor success rate for long-term weight reduction. Most obese people eventually regain the weight they have worked so hard to lose. Weight regain has emerged as one of the most significant obstacles for obesity therapeutics, undoubtedly perpetuating the epidemic of excess weight that now affects more than 60% of U.S. adults. In this review, we summarize the evidence of biology's role in the problem of weight regain. Biology's impact is first placed in context with other pressures known to affect body weight. Then, the biological adaptations to an energy-restricted, low-fat diet that are known to occur in the overweight and obese are reviewed, and an integrative picture of energy homeostasis after long-term weight reduction and during weight regain is presented. Finally, a novel model is proposed to explain the persistence of the "energy depletion" signal during the dynamic metabolic state of weight regain, when traditional adiposity signals no longer reflect stored energy in the periphery. The preponderance of evidence would suggest that the biological response to weight loss involves comprehensive, persistent, and redundant adaptations in energy homeostasis and that these adaptations underlie the high recidivism rate in obesity therapeutics. To be successful in the long term, our strategies for preventing weight regain may need to be just as comprehensive, persistent, and redundant, as the biological adaptations they are attempting to counter. energy restriction; diet-induced obesity; obesity prone; weight loss; energy balance IN THE UNITED STATES, OVER 60% of adults and close to 20% of children are overweight or obese (35,174). A number of effective weight loss strategies are available, but most are only transiently effective over a period of 3 to 6 mo. Less than 20% of individuals that have attempted to lose weight are able to achieve and maintain a 10% reduction over a year (128). Over one-third of lost weight tends to return within the first year, and the majority is gained back within 3 to 5 years (3,246). A number of reasons have been proposed for the high incidence of weight regain (69,246), and several point to the biological response to weight loss.The objective of this review is to examine the role of this biological response in the process of weight regain. Biological regulation is first discussed in relation to other nonbiological pressures that affect body weight as weight is gained, lost, and regained. The specific biological adaptations to the most common form of dieting, an energy-restricted low-fat diet, are then discussed in more detail. Previous reviews provide extensive descriptions of the normal adaptive response to energy restriction. We do not attempt to recapitulate those efforts here. Rather, the unique perspective of this review summarizes those adaptations that have been confirmed o...

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“…[9][10][11] Insulin resistance (IR) is involved and insulin-sensitivity improvement is maintained in obese patients for 2-3 years after dietary weight loss if weight is not regained. 12,13 The observation of a paradoxical increase of insulin sensitivity in animals infected by Ad36 14 is intriguing and envisages the possibility that a better glycemic control in Ad36-infected subjects could be achieved. The mechanisms involved appear to lead to expansion of adipose tissue and increase of glucose uptake in skeletal muscle and adipose tissue, which collectively might lead to better glycemic control in vivo.…”

Section: Introductionmentioning

confidence: 99%

Human obesity relationship with Ad36 adenovirus and insulin resistance

et al. 2009

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Objectives: Infection with specific pathogens may lead to increased adiposity: a specific adiposity-promoting effect of Ad36 human adenovirus, without the involvement of neurological mechanisms, was reported. The aim of this study is to investigate whether non-diabetic patients with earlier Ad36 infection show greater degrees of overweight obesity, of Insulin Resistance (IR), assessed by homoeostasis-model assessment (HOMA), and/or of other related factors. Moreover, the relationship, if any, among these factors and an earlier Ad36 infection, and the hypothesis of a mechanism involving IR are investigated. Subjects: Ad36 seropositivity is assessed in 68 obese and 135 non-obese subjects, along with body composition, HOMA and laboratory investigations. Results: Age, body mass index (BMI), waist-hip ratio, blood pressure, insulin, HOMA and triglycerides are significantly greater in the Ad36 seropositive group. Ad36 seropositivity, along with HOMA and total cholesterol, explains BMI variance. No Ad36 seropositivity effect to HOMA could be envisaged by the same statistical model. Conclusion: A significant association of Ad36 seropositivity with obesity and with essential hypertension in human beings is suggested by our study; this association is mostly significant in women. Our results do not support that any Ad36 adipogenic adenovirus effect is operating in human obesity through an insulin-resistance-related mechanism. Ad36 seropositive status could also be a hallmark of a clinical-metabolic profile possibly preceding obesity and diabetes in non-obese patients.

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Persistence of improvement in insulin sensitivity following a dietary weight loss programme

Cited by 27 publications

References 33 publications

Adenovirus-36 Seropositivity Enhances Effects of Nutritional Intervention on Obesity, Bright Liver, and Insulin Resistance

Adenovirus-36 Seropositivity Enhances Effects of Nutritional Intervention on Obesity, Bright Liver, and Insulin Resistance

Biology's response to dieting: the impetus for weight regain

Human obesity relationship with Ad36 adenovirus and insulin resistance

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